Glossary of Hypercoagulable state
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- mass of clot free in blood
- blockage of blood vessel
- Ischemic necrosis
- death due to lack of blood flow
- necrotic area
- Why are thrombus formations life threatening?
- Clots may dislodge/cause occlusion or infarct.
- Why are thrombi life-saving?
- 1. Stop bleeding
2. Maintains homeostasis
- What factors pre-dispose a patient to thrombosis?
- 1. Injury to endothelium
2. Altered blood flow
3. Altered hemostatic systems
- What are 5 therapeutic measures for thrombosis?
- 1. Low dose heparin
2. Full dose coumadin
5. Physical therapy
- 2 Inhibitors of Fibrinolysis
- 4 Inhibitors of Coagulation
- Activator of Fibrinolysis
- Plasmin activation
- Activator of Coagulation
- 8 Risk factors for Thrombosis
- 4 Challenges causing Thrombosis
- 1. Injury
- What general lab results accompany thrombosis?
- 1. History
2. PT/PTT - normal to sl. low
3. NORMAL bleeding time
4. NORMAL platelet count
- What are the 4 more common hereditary disorders of hypercoagulation?
- 1. Protein C defic.
2. Protein S defic.
3. ATIII defic.
4. APC resistance
- What are the similar features of the four hereditary disorders?
- 1. All autosomal dominant
2. All cause DVT
- Which disorders have earliest onset?
- Proteins C/S - at birth in homozygotes
- Which disorders have earliest onset at adolescence?
- Proteins C/S - heterozygotes
ATIII - Heterozygotes
- When does APC resistance become apparent in patients?
- Homozygotes - age 10-40
Heterozygotes - about 40
- Which disorder can cause:
- Super-thrmbophleb = Protein S
purpura fulminans = Protein C
- What's the only difference btwn PRotein C/S disorders?
- -S causes pulmonary embolism and thrombophlebitis
-C causes purpura fulminans.
-Homozygous C is fatal
- What causes PRotein S deficiency?
- -Congenital - genetics
-Acquired - Vit K defic, Liver disease
- Why does warfarin/coumadin therapy induce protein s/c deficiency?
- They have shorter t1/2's than other factors, so decrease faster; leaves patient at risk for thrombosis.
- -What does Factor V leiden deficiency cause?
-What causes it?
- -APC resistance
-Congenital - genetics
- What is the main problem in APC resistance?
- -A point mutation of factor five; unable to be inactivated by APC.
- What 2 types of screening tests are used for APC resistance?
- 1. Clot based - PT/APTT
- What test is used to confirm APCR?
- PCR on isolated DNA
- What is the principle of the aPTT for Fx V leiden?
- -Fx V deficient plasma + Pt.
-If prolonged, Fx V is ok
-If not, Fx V is resistant.
- What type of APCR is more common; hetero or homozygous?
- Homozygous - 50-100%
Hetero = 5-10%
- What are 7 results of Thrombosis?
- 1. Deep vein thrombosis
2. pulmonary embolism
3. recurrent pregnancy loss
4. Myocardial infarct
7. Post-op thrombosis
- What are the 3 main lab criteria for diagnosing LA?
- -Abnormal PT
-Prolonged PTT that doesn't correct
- What is the LA basically?
- An Antiphospholipid Antibody.
- What are non-lupus causes of anticardiolipin antibody?
-immune thrombocytopenic purpura
- What are the 2 more common causes of deep vein thrombosis?
- -LA - 8-14%
-Factor V Leiden 40-50%
-Protein S = 5%
-PC/ATIII = 3%
- why are the pt/ptt prolonged in LA states?
- -They inhibit clotting in vitro by attacking actin; but not in vivo.
- What are 3 types of tests for LA?
- 1. Increased phospholipid (sta-clot)
2. Decreased phospholipid
3. Specific Elisas for IgG/M
- What is the basic principle of the StaClot procedure?
- 1. 2 tubes incubated; one w/ hexagonal phase phospholipid.
2. Run aPTT on both; the HPE will neutralize LA if present
3. Compare clotting times.
- What tests specifically detect LA's?
- -LA screen
- What is the reagent in LA tests?
- Dilute Russell's viper venom
- What is the principle of the DRVVT LA-screen?
- -Viper venom activates Fx X
-Bypasses VII/factors above 9/8 in intrinsic.
-Specific b/c less affected by factor deficiencies or inhibitors.
- What happens in the LA confirm?
- -More procoag phospholipid is put in to neutralize LA.
-Polybrene also added for heparin resistance.
- Why would heparin interfere with LA testing?
- Of course the PPT would be prolonged and uncorrected.
- What's another name for inhibitor assays?
- mixing studies
- what is the principle of mixing studies?
- -mix suspect plasma w/ PPP.
-If it doesnt correct, or is prolonged after incubation, confirm w/ factor assays.
- NAME THE:
-Increased phospholipid test
-Decreased phospholipid test
- Incr = StaClot
Decr = LA COnfirm
- So when do we test for inhibitors?
- When PT/PTT are prolonged by:
-other factor inhibitors
- If PT AND aPTT are abnormal and uncorrectable:
- contamination, probly heparin
- What 3 therapeutic agents given to patients with LA?
-LMWH if pregnant
- What 2 miscellaneous thrombotic disorders must i know?
- 1. Hyperhomocysteinemia
2. Prothrombin mutations
- What causes hyperhomocystin?
- -Vascular toxin
- What should i remember about prothrombin mutations?
- -Test with PCR
-Lifelong Warfarin therapy
- If not a factor disorder or circulating anticoagulant, what can alter fibrinolysis?
- 1. Plasminogen deficiency
3. Increased PAI-1
- what is PAI-1?
- Tissue plasminogen activator inhibitor - keeps the activation of plasminogen in check.
- What causes plasminogen deficiency?
- Autosomoal dominant inheritance.
- How is plasminogen deficiency tested for?
- Functional antigen assay
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